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LncRNA CEBPA-AS1 Overexpression Inhibits Proliferation and Migration and Stimulates Apoptosis of OS Cells via Notch Signaling.

ABSTRACT: Osteosarcoma (OS) is the most common primary bone malignancy derived from primitive bone-forming mesenchymal cells. Long noncoding RNA (lncRNA) expression profiles have been intensively studied for their involvement in OS. Herein, we clarify whether lncRNA CEBPA-AS1 is a regulator of NCOR2 in OS cells. Microarray-based expression analysis identified OS-related differentially expressed lncRNA and predicted microRNAs (miRs) binding to lncRNA and mRNA. lncRNA CEBPA-AS1 and NCOR2 were found to be weakly expressed in OS tissues and cells. Next, functional investigation revealed that lncRNAs CEBPA-AS1 bound to miR-10b-5p to upregulate NCOR2. Following that, gene-targeted knockdown and overexpressed recombinant vectors of lncRNA CEBPA-AS1 and NCOR2 were constructed to explore the effects of lncRNA CEBPA-AS1 and NCOR2 on cell proliferation, differentiation, migration, and apoptosis. Finally, tumor formation was measured in nude mice. lncRNA CEBPA-AS1 overexpression or NCOR2 elevation inhibited cell proliferation and migration, and alkaline phosphatase (ALP) and bone gla protein (BGP) activity, while enhancing apoptosis and tumor formation. Furthermore, NCOR2 was elevated in response to lncRNA CEBPA-AS1 overexpression, thus repressing the Notch signaling pathway. Taken together, lncRNA CEBPA-AS1 overexpression inhibits OS progression through diminishing activation of the Notch signaling pathway via upregulating NCOR2. Therefore, lncRNA CEBPA-AS1 may serve as a molecular target for treating OS.

SUBMITTER: Xia P

PROVIDER: S-EPMC7056609 | biostudies-literature |

REPOSITORIES: biostudies-literature

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Project description:BackgroundLong non-coding RNAs (lncRNAs) are pervasively transcribed in genome and emerging as a new player in tumorigenesis due to their functions in transcriptional, posttranscriptional and epigenetic mechanisms of gene regulation. As the most frequent malignancy and the foremost source of cancer mortality, lung cancer is a heterogeneous disorder. The most common type of lung cancer is Non-small cell lung cancer (NSCLC), occupying 85% of the total cases, and the main subtypes of NSCLC include lung adenocarcinoma (LAD), large cell carcinoma (LCC), and lung squamous cell carcinoma (LSCC). Recently, numerous lncRNAs have been reported to be strongly linked to NSCLC. In the present study, we found that a new lncRNA CBR3-AS1 is highly expressed in lung cancer. In addition, we also examined the expression of lncRNA CBR3-AS1 in 60 of LADs, 40 of LCCs and 40 of LSCCs patient samples, finding that CBR3-AS1 was specificity highly expressed in LAD cancer tissues. Mechanically, we discovered that CBR3-AS1 could regulate the proliferation, migration and invasion of LAD cells through targeting Wnt/β-catenin signaling.MethodsReal-time PCR, RNA-pulldown, RIP, western blotting, lentivirus transfection, luciferase reporter assays, cell proliferation assays, colony formation assays, wound healing scratch assays and transwell assays were employed to examine the relationship between lncRNA CBR3-AS1 and its regulation of Wnt/β-catenin signaling in LAD cells.ResultsLncRNA CBR3-AS1 is highly-expressed in LAD and cell lines. LncRNA CBR3-AS1 shows physical association with β-catenin. CBR3-AS1 could facilitate Wnt/β-catenin signaling activation thought promoting nuclear localization of β-catenin. CBR3-AS1 promotes LAD cell proliferation, migration and invasion by targeting Wnt/β-catenin signaling.ConclusionIt can be found that a new functional lncRNA CBR3-AS1 could promote nuclear localization of β-catenin so as to facilitate Wnt/β-catenin signaling activation and regulate the proliferation, migration and invasion of LAD cells.

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LncRNA CEBPA-AS1 Overexpression Inhibits Proliferation and Migration and Stimulates Apoptosis of OS Cells via Notch Signaling.

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